Danshensu attenuates aldosterone-induced cardiomyocytes injury through interfering p53 pathway.

Heart failure, characterized by impaired systolic and/or diastolic function, is a common cardiovascular disease. The loss of cardiomyocytes due to various factors, including through necrosis or apoptosis can result in heart failure. Previous studies have indicated that excessive aldosterone (ALD) serves an essential role in the process of heart failure, and the heart is also one of the direct targets of ALD, which can provoke hypertrophy and the apoptosis of cardiomyocytes. The aim of the present study was to investigate the protective effect of danshensu (DSS) on ALD‑induced cardiomyocytes injury. The present results demonstrated that DSS increased cell viability and decreased the leakage of lactate dehydrogenase in cardiomyocytes exposed to ALD. In addition, DSS decreased the apoptotic rate of ALD‑stimulated cells. Further research indicated that DSS‑ and cellular tumor antigen p53 (p53)‑alone or combination treatment was able to decrease the expression levels of apoptosis regulator BAX and caspase‑3, and increase the expression of apoptosis regulator B‑cell lymphoma (Bcl)‑2 in ALD‑stimulated cardiomyocytes. Taken together, the results of the present study suggest that DSS inhibits the harmful effects of ALD on cardiomyocytes via interfering with the p53 signaling pathway. These results provide novel evidence for the potential protective effects of DSS.